| Project/Area Number | 01480194 |
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | Juntendo University School of Medicine |
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Principal Investigator |
OKUMURA Ko Juntendo University, Professor, 医学部, 教授 (50009700)
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| Co-Investigator(Kenkyū-buntansha) |
OBATA Tetsuji Juntendo University, Associate Professor, 医学部, 講師 (10205445)
YAGITA Hideo Juntendo University, Associate Professor, 医学部, 助教授 (30182306)
屋部 登志雄 順天堂大学, 医学部, 助手 (50239836)
中村 哲也 順天堂大学, 医学部, 助手 (30189047)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed(Fiscal Year 1991)
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| Budget Amount *help |
¥5,700,000 (Direct Cost : ¥5,700,000)
Fiscal Year 1991 : ¥1,300,000 (Direct Cost : ¥1,300,000)
Fiscal Year 1990 : ¥1,200,000 (Direct Cost : ¥1,200,000)
Fiscal Year 1989 : ¥3,200,000 (Direct Cost : ¥3,200,000)
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| Keywords | LFA / VLA / mAb / lymphocyte / tolerance / lymphocyte / CD2 / TcR / トランスフェクタント / CD4 |
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| Research Abstract |
Cell interactions in the immune system are mediated by several different families of receptors on cell surface, and these adhesion molecules influence many diverse processes including, differentiation, migration and cellular activation. To understand in vivo significance of these molecules in various and immunological phenomenon, we have been mainly, focussing murine as well as rat experimental systems. We report the experimental results performed to understand the role of VLA-4, LFA-1, and ICAM-1 in cell migration and activation in rat and mouse experimental systems.
(1) Anti-rat VLA-4 mAb, which we established, could inhibit lymphocyte homing to Payeris patch selectively.
(2) Anti-rat VLA-4- mAb inhibited the infiltration of lymphocytes, monocytes and eosinophils but not neutrophils to inflamatory sites.
(3) Fibronectin acted costimulatory in FceRI-mediated activation of rat mast cells. This costimlatory effect was mainly mediated by VLA-4.
(4) Anti-VLA-4 mAb prevented the cardiac allograft rejection more strongly than anti-LFA-1 mAb.
(5) Mixed administration of inti-LFA-1 and anti-ICAM-1 mAbs caused specific cardiac allograft tolerance in both murine and rat systems.
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